We report a case of leukocytoclastic vasculitis (LCV) in a 74-year-old woman, occurring seven months after the initiation of fluoxetine therapy for generalized anxiety disorder (GAD). The cutaneous lesions resolved upon discontinuation of fluoxetine but recurred promptly upon rechallenge. Notably, subsequent exposure to paroxetine, another selective serotonin reuptake inhibitor (SSRI) previously tolerated by the patient, also elicited a similar but less severe rash, suggesting cross-sensitization. Transition to venlafaxine, a serotonin-norepinephrine reuptake inhibitor (SNRI), led to complete and sustained resolution of the skin lesions. This case highlights three key clinical points: the potential for delayed-onset cutaneous adverse reactions to SSRIs even after months of uneventful treatment; the occurrence of cross-reactive hypersensitivity among SSRIs; and the importance of considering alternative antidepressant classes with distinct pharmacological profiles in patients with SSRI-associated vasculitis.

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a rare, potentially life-threatening immune-related adverse event that can be triggered by immune checkpoint inhibitors. We present the case of a 58-year-old woman with malignant acral melanoma who developed late-onset DRESS following sequential treatment with pembrolizumab and nivolumab. The patient initially developed a generalized erythrodermic, scaly rash with pruritus after the third dose of pembrolizumab, which recurred upon switching to nivolumab. Laboratory evaluation revealed leukocytosis, marked eosinophilia, transaminitis, and elevated lactate dehydrogenase. Skin biopsies demonstrated spongiosis, basal vacuolar degeneration, eosinophilic infiltrate, and leukocytoclastic vasculitis, consistent with DRESS. Despite corticosteroid therapy, the patient experienced multiple relapses triggered by immunosuppressant tapering, requiring prolonged cyclosporine treatment. Her presentation met the registry of severe cutaneous adverse reactions (RegiSCAR) criteria for definite DRESS. This case underscores the need for heightened awareness of delayed hypersensitivity reactions to immune checkpoint inhibitors and highlights the possibility of a chronic-relapsing course requiring extended immunosuppressive therapy.

Angiotensin-converting enzyme (ACE) inhibitor-associated hypersensitivity vasculitis with gastrointestinal involvement is an uncommon but important drug-related cause of acute abdominal pain and may mimic an acute surgical abdomen. We report the case of an 84-year-old man admitted for redo aortic valve replacement following infective endocarditis, who developed acute abdominal pain on postoperative day 14. Physical examination revealed diffuse abdominal tenderness and cutaneous purpura. Laboratory testing showed elevated inflammatory markers with peripheral eosinophilia. Contrast-enhanced abdominal CT demonstrated concentric small bowel wall thickening with submucosal edema and ascites, without evidence of mesenteric ischemia. Skin biopsy confirmed leukocytoclastic vasculitis. Lisinopril was initiated at the time of admission and continued throughout the perioperative period; symptoms occurred approximately three weeks after treatment initiation, with no prior history of similar episodes. Discontinuation of lisinopril resulted in rapid clinical improvement and complete resolution of abdominal symptoms. This case highlights that ACE inhibitor-associated hypersensitivity vasculitis may present with small bowel edema and imaging findings overlapping with intestinal angioedema. Careful medication review and recognition of associated systemic features such as purpura and eosinophilia are essential to avoid unnecessary invasive procedures.

Cite this article as: Günegül Y, Tozlu M, Demiral YE, Eminler AT, Uslan Mİ. Leukocytoclastic vasculitis occurring during upadacitinib therapy in ulcerative colitis: A case report. Turk J Gastroenterol. 2026;37(4):529-531.

BACKGROUND Dalbavancin is a lipoglycopeptide antibiotic largely used to treat serious and complex bacterial infections, particularly those caused by gram-positive bacteria. Its main advantages include a prolonged half-life, which allows for once-weekly dosing, effectiveness against resistant pathogens, most notably, methicillin-resistant Staphylococcus aureus, and a good profile of tolerability and patient adherence. Herein we report the first documented case of a patient who developed palpable purpura on both lower limbs following treatment with dalbavancin, which was clinically and histologically diagnosed as leukocytoclastic vasculitis (LV). CASE REPORT A 66-year-old woman received dalbavancin due to an acute bacterial skin and skin structure infection (ABSSSI) of her right leg. The patient initially showed a favorable clinical response, with marked improvement of the infection. However, 3 weeks after the administration of dalbavancin, she developed a diffuse erythematous palpable purpura, predominantly affecting the lower limbs, and accompanied by mild arthralgia and generalized asthenia. To further investigate and confirm the underlying cause of these new symptoms, a skin biopsy was performed, revealing histopathological findings consistent with LV. Following the diagnosis, corticosteroid therapy was initiated, resulting in a significant symptomatic improvement. CONCLUSIONS To the best of our knowledge, this is the first published, histologically confirmed case report of LV developing after treatment with dalbavancin. Given the widespread use of dalbavancin for treating ABSSSIs, clinicians should be aware of the potential adverse effects, including LV, that may arise during its administration.

Vancomycin is a first-line antibiotic used for severe gram-positive infections, but it may rarely trigger immune-mediated small-vessel vasculitis. We report a case of a 43-year-old man with end-stage renal disease on home hemodialysis who developed palpable purpuric skin lesions three days after starting vancomycin for L5-S1 discitis and osteomyelitis. Over the following days, the eruption progressed into symmetric, non-blanching purpuric plaques involving the upper and lower extremities by day 6 of therapy. Laboratory evaluation demonstrated progressive thrombocytopenia, an increase in eosinophil counts within the normal reference range, and elevated inflammatory markers, which declined after vancomycin cessation. Vancomycin was discontinued, and antimicrobial therapy was transitioned to daptomycin, resulting in rapid clinical improvement within 48 hours and near-complete resolution by day 12. This case emphasizes the importance of early recognition of vancomycin-induced leukocytoclastic vasculitis, particularly in patients with renal impairment who may experience an accelerated onset. Prompt discontinuation of the offending agent typically results in rapid recovery without the need for systemic corticosteroids.

Digital necrosis is now a well-established complication of COVID-19 infection, but data are sparse regarding the pathophysiology. We present the case of digital necrosis secondary to cutaneous leukocytoclastic vasculitis in a patient with COVID-19 infection. After histologic confirmation of vasculitis, the patient was given methylprednisolone leading to an improvement that enabled limited amputation.

Coumarin derivatives, including warfarin and acenocoumarol, are widely used oral anticoagulants that inhibit vitamin K-dependent coagulation factors. They are commonly prescribed for the prophylaxis of thromboembolic disorders. Although effective, these agents are associated with many adverse drug reactions, which include hemorrhagic complications, warfarin-induced skin necrosis, hypersensitivity reactions, and, rarely, leukocytoclastic vasculitis (LCV). LCV is an immune-mediated small-vessel vasculitis characterised by palpable purpura, often triggered by drugs, infections, or autoimmune conditions. Here, we present the case of a 53-year-old female with a history of rheumatic heart disease and mechanical mitral valve replacement who developed LCV after 5 years on acenocoumarol. The reaction persisted despite adjunct therapy and worsened upon switching to warfarin, suggesting possible cross-reactivity between these coumarin derivatives. Ultimately, transitioning to apixaban led to the complete resolution of symptoms. This case underscores the importance of early recognition of drug-induced vasculitis and highlights the need for individualised anticoagulation strategies in patients with hypersensitivity reactions.

Herpes zoster is well-known for its association with large-vessel vasculitis, particularly in the central nervous system. This report highlights a rare diagnosis of small-vessel cutaneous leukocytoclastic vasculitis linked to herpes zoster. A 73-year-old man, during an extended ICU stay following an anterior myocardial infarction complicated by respiratory failure, developed a self-limiting bullous rash. Biopsy revealed epidermal infection by varicella-zoster virus (confirmed through immunohistochemistry and histologic morphology) accompanied by dermal leukocytoclastic vasculitis. This represents the 14th documented diagnosis of small-vessel leukocytoclastic vasculitis associated with varicella-zoster infection. This report broadens the spectrum of herpes zoster presentations, particularly in immunocompromised patients, and provides a valuable reference for clinicians managing atypical manifestations of this infection.

We report the case of a 57-year-old male presenting with severe, recurrent perineal angioedema and cutaneous leukocytoclastic vasculitis, both of which manifested shortly after commencing lisdexamfetamine for attention deficit hyperactivity disorder. A positive rechallenge after an extensive workup confirmed a drug-induced reaction. This case highlights lisdexamfetamine as a cause of non-allergic angioedema and leukocytoclastic vasculitis, and demonstrates the diagnostic value of a medication history and rechallenge.

Monoclonal gammopathy (MG) associated with dermatological disorders, which is classified as monoclonal gammopathy of clinical significance (MGCS), represents a well-established complication. These dermatologic conditions are linked to the infiltration and proliferation of malignant plasma cells or the deposition of monoclonal immunoglobulin in nonmalignant monoclonal gammopathy. Immunoglobulin light chain amyloidosis (AL amyloidosis) is a clonal, non-proliferative plasma cell disorder characterized by the deposition of fragments of immunoglobulin light chains in tissues. Erythema elevatum diutinum (EED) is clearly associated with monoclonal gammopathy, particularly IgA monoclonal gammopathy, although the pathomechanism has not been clearly established. In this article, we report an extremely rare case involving the coexistence of cutaneous light chain amyloidosis (AL amyloidosis) and erythema elevatum diutinum (EED) as the presenting features of IgA monoclonal gammopathy, which to our knowledge is the first reported case. During a 5-year follow-up period, intermittent occurrence of skin lesions persisted without significant changes observed in blood system examinations. Furthermore, we provided a comprehensive review of the existing literature on EED associated with IgA MG to enhance the understanding of skin significance of MG.